Gastroparesis in a patient with diabetes . Left posterior oblique view of the stomach from a single-contrast upper GI examination shows a flaccid, mildly dilated stomach. There was no gastric peristalsis at fluoroscopy. Nevertheless, barium is seen to empty from the stomach into the duodenal bulb (arrows) without evidence of gastric outlet obstruction
Gastroparesis in a patient on narcotic medication for chronic low back pain.
Supine view from a single-contrast upper GI examination shows a flaccid stomach with delayed emptying of barium into the duodenum. There was no gastric peristalsis at fluoroscopy.
Repeat view later in the study shows emptying of barium into the duodenal bulb and descending duodenum (arrows) without evidence of gastric outlet obstruction
Gastroparesis in a patient with hypothyroidism . Left posterior oblique view from a double-contrast upper GI examination shows a considerably dilated stomach with retained intraluminal fluid causing flocculation of ingested barium. There was markedly decreased gastric peristalsis at fluoroscopy. Despite these findings, note barium in the duodenal bulb and descending duodenum (arrows) without evidence of gastric outlet obstruction
Idiopathic gastroparesis in a young woman. An upright frontal view from a single-contrast upper GI examination shows a barium level (black arrows) in the gastric antrum and a fluid level (white arrows) in the upper gastric body due to gastroparesis with markedly delayed emptying of fluid and secretions from the stomach. Also note the absence of any barium in the duodenum on this early image from the study
Gastroparesis in a patient with diabetes . There is a large amount of retained food/debris (white arrows) in the stomach secondary to marked gastroparesis. Also note several food particles (black arrows) in the duodenal bulb. Despite retention of undigested food in the stomach, there is normal emptying of barium into nondilated duodenum and proximal small bowel without evidence of gastric outlet obstruction
Surprisingly, in the study by Levin et al., seven (35%) of 20 patients with gastroparesis who underwent nuclear medicine solid gastric emptying scans had normal emptying of solids from the stomach . Four of these patients were treated for gastroparesis and three (75%) had symptomatic improvement, suggesting that they had gastroparesis despite normal emptying of solids on the nuclear scans. These findings support the observations of other investigators that delayed gastric emptying of solids on a nuclear medicine scan is not a prerequisite for the diagnosis of gastroparesis [26, 27]. These discrepancies can be explained by the fact that delayed emptying of solids from the stomach is one marker for gastroparesis and that decreased or absent gastric peristalsis is another marker for an overlapping group of patients with this condition.
Gastric bezoars , defined as conglomerate masses of food or foreign matter in the stomach, have a reported incidence of less than 1% in the general population . Bezoars classically have been attributed to ingestion of fruit or vegetable matter (especially persimmons) that form conglomerate masses, also known as phytobezoars , or to ingestion of hair that forms matted hair balls, also known as trichobezoars , in the stomach [34–36]. However, most gastric bezoars are now believed to be caused either by gastroparesis [37–41] or by partial gastrectomy [42–44] or bariatric surgery [41, 45–47]. Whatever the underlying cause, decreased or absent gastric peristalsis results in poor mechanical breakdown of ingested solids that go on to form conglomerate masses of undissolved food matter in the stomach. In one study, 58% of patients with gastric bezoars had known risk factors for gastroparesis, and barium studies revealed markedly decreased or absent peristalsis in the stomach in 62% of patients who had not undergone partial gastric resection or bariatric surgery .
It is well recognized that gastric bezoars may develop as a complication of partial gastrectomy for gastric ulcers or other abnormalities [42–44]. Such bezoars are thought to develop as a result of gastric resection and vagotomy, with loss of gastric peristalsis and the normal mixing function of the distal part of the stomach [42, 43]. Such bezoars have been shown to occur after partial gastrectomy even in the absence of anastomotic strictures (Fig. 29.6), so these bezoars presumably develop because of surgical absence of the gastric antrum and body—the portion of the stomach normally responsible for breaking down ingested solids by active peristalsis. Thus, even in the absence of anastomotic strictures, these patients have the functional equivalent of severe gastroparesis as the cause of bezoar formation.
Gastric bezoar after partial gastrectomy and gastrojejunostomy for ulcer disease. The bezoar is seen as a large conglomerate mass of undigested food (black arrows) in the gastric remnant. Despite the bezoar, this patient has a patent gastrojejunal anastomosis (white arrows) without evidence of anastomotic obstruction
Similarly, patients who undergo bariatric procedures such as Roux-en-Y gastric bypass or laparoscopic gastric banding may develop bezoars within the gastric pouch even in the absence of strictures or obstruction of the pouch (Fig. 29.7), presumably because of surgical bypass of the gastric antrum and body or laparoscopic banding of the proximal stomach that delays emptying of ingested food into the antrum and body (where gastric peristalsis normally occurs), so these patients also have the functional equivalent of severe gastroparesis [41, 45–47]. With the rising popularity of bariatric surgery for treatment of morbid obesity, gastric bezoars are likely to be encountered with greater frequency as a complication of this surgery in the future.
Gastric bezoar after Roux-en-Y gastric bypass . A large radiolucent bezoar (short black arrows) is present within the gastric pouch. Note emptying of barium from the pouch into the jejunum (long white arrows) via a patent gastrojejunal anastomosis (short white arrow). Also note barium entering the excluded gastric body/antrum (long black arrows) secondary to breakdown of the gastric staple line
Patients with gastric bezoars may present with a variety of symptoms, including epigastric pain, bloating, nausea, vomiting, early satiety, upper GI bleeding, or even intermittent dysphagia caused by mobile bezoars that periodically obstruct the gastric cardia [37, 41, 48]. The development of intractable symptoms occasionally necessitates treatment by dissolution or suction of the bezoar at endoscopy.
While bezoars might be expected to develop slowly over a long period of time, it has been shown that some patients have symptoms for less than 1 week and that bezoars can resolve quickly on dietary restrictions and pharmacologic agents without need for endoscopy . Thus, some patients with gastric bezoars have an acute clinical presentation, and some bezoars can heal rapidly on conservative management.
Gastric bezoars classically appear on barium studies as mobile masses in the stomach that float in the barium pool and typically have a mottled appearance secondary to trapping of barium in the interstices of the mass (Fig. 29.8) . However, some gastric bezoars have a more homogeneous appearance (Fig. 29.9) or can be immobile at fluoroscopy if they are adherent to the gastric wall . Rarely, bezoars can become so large that they occupy virtually the entire stomach (Fig. 29.10) . Even when freely mobile, bezoars may sink to the most dependent portion of the barium pool (rather than floating in the barium pool) because of their high density . As a result, gastric bezoars can be manifested by a spectrum of findings on barium studies, depending on their cohesiveness and density. It therefore is important to recognize the value of barium studies with real-time fluoroscopy for assessing the appearance and mobility of a bezoar and its relationship to the gastric lumen.
Giant gastric bezoar in patient with underlying gastroparesis. The bezoar is seen as a large conglomerate mass of undigested food (black arrows) in a dilated stomach. Note the mottled appearance of the bezoar secondary to trapping of barium in the interstices of the mass. Also note barium in the duodenum and proximal jejunum (white arrows) without evidence of gastric outlet obstruction
Gastric bezoar filling virtually the entire stomach as a giant conglomerate mass of undigested food. Also note food within the lumen of a small hiatal hernia (arrows)
Competitive Speed Eating
Competitive speed eating has emerged over the past decade as an increasingly popular competitive sport with a growing legion of worldwide fans. These contests raise a fascinating question about how speed eaters are able to consume such enormous quantities of food in such short periods of time. In a study by Levine et al. from 2007 , this issue was addressed in a speed eating simulation with fluoroscopic observation of a professional speed eater ranked as one of the top competitors in the world by the International Federation of Competitive Speed Eating (IFOCE). The speed eater was found to have markedly altered gastric motility at fluoroscopy, as his stomach rapidly accommodated an enormous quantity of ingested food by progressively expanding until it became a giant, flaccid sac occupying a major portion of his abdomen (Fig. 29.11). Put differently, his stomach acted as a compliant, expansile receptacle, dilating to a degree that it could accept an almost unlimited volume of food. Conversely, gastric peristalsis was virtually absent at fluoroscopy, and little or no ingested food emptied into the duodenum. Though the simulation involved only a single speed eater, the fluoroscopic findings were so spectacular that the investigators postulated that the profound gastroparesis observed in their subject could be extrapolated to speed eaters in general as the basis for their speed eating skills .
Competitive speed eater’s stomach after consuming 36 hot dogs in a speed-eating simulation. The stomach is filled with undigested hot dog pieces and has expanded to form a giant, flaccid sac (white arrows) occupying a major portion of his upper and midabdomen. Nevertheless, a small amount of barium is seen to enter the proximal duodenum (black arrows) without evidence of gastric outlet obstruction
On subsequent questioning, the speed eater indicated that he developed his speed-eating skills by extensive training, forcing himself to consume ever-increasing amounts of food despite a sensation of satiety . In effect, he was able to overcome the usual checks and balances associated with eating by exercising extreme self-discipline to consume larger and larger quantities of food than “normal” eaters could ever ingest. Only as a result of this prolonged and intensive training was the speed eater able to adapt his stomach until it could withstand the rigors of competitive speed eating. In that sense, a world-class speed eater requires a level of commitment and will power comparable to those of professional athletes honing their skills for other sports.
Nevertheless, the investigators who performed the simulation expressed concern that a chronically dilated, flaccid stomach with profound self-induced gastroparesis could eventually decompensate, becoming an enormous sac incapable of shrinking to its normal size and incapable of peristalsing and emptying solid food . If so, long-term competitive speed eaters could develop intractable nausea and vomiting, potentially necessitating a partial or total gastrectomy to relieve their symptoms and restore their ability to eat normally . In this context, competitive speed eating could be viewed as a self-destructive form of behavior, so competitive speed eaters need to be aware of the potential long-term risks of this sport.
Question #2: When patients with nausea and vomiting experience immediate retching and emesis of ingested barium on upper GI barium studies, should the examination be aborted or does it still have a potential role in determining the cause of nausea and vomiting in these patients?
When patients with recurrent nausea and vomiting have immediate retching and emesis of ingested barium on an upper GI barium study, some radiologists erroneously assume that there will not be an adequate volume of barium in the stomach to obtain a diagnostic examination. It turns out, however, that even a small amount of residual barium in the stomach often enables differentiation of gastric outlet obstruction or gastroparesis from extraintestinal causes of recurrent nausea and vomiting, such as narcotics, chemotherapy, acute infectious conditions, seizures, increased intracranial pressure, and vestibular disorders. Patients with gastric outlet obstruction or gastroparesis typically have a dilated stomach with intraluminal fluid and/or food that dilutes ingested barium and delays emptying of barium into the duodenum and proximal small bowel. In contrast, patients with extraintestinal causes of nausea and vomiting typically have a collapsed or partially collapsed stomach with rapid emptying of residual barium into collapsed or partially collapsed duodenum and proximal small bowel. In such patients, the combination of rapid emesis of ingested barium and a collapsed stomach with rapid emptying of residual barium from the stomach have led to the designation of a so-called “hyperirritable” stomach . These findings therefore should prompt a careful search for extraintestinal causes of nausea and vomiting in affected individuals. The following section discusses in greater detail the predisposing factors as well as the clinical and radiographic findings in patients with a hyperirritable stomach.